The overall goal of this project is to determine how androgens influence protein metabolism in two model systems in which genetic defects alter hormonal response. In the mouse kidney, beta-glucuronidase is an index of androgen responsiveness. This protein is of particular interest since it has one of the best mapped eukaryotic genes. The use of genetic mutants which alter the rate of synthesis of beta-glucuronidase will allow a direct analysis of how the mgnitude of androgen response is governed. In addition, testosterone (and FSH) induced androgen binding protein (ABP) will be studied in normal and Hre rats. These latter animals have genetically determined seminiferous tubular failure which probably is the consequence of a Sertoli cell defect. As a result, turnover studies of a Sertoli cell marker protein such as ABP could provide insight into the nature of this gene defect. The recent isolation of homogeneous ABP and preparaion of a radioimmunoassay suitable for tissue and blood will facilitate these studies.